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Table of Contents
Vol. 16, No. 2-3, 2008
Issue release date: February 2008
Section title: Paper
Neurosignals 2008;16:154–164

Opposing Roles for Reactive Astrocytes following Traumatic Brain Injury

Laird M.D. · Vender J.R. · Dhandapani K.M.
Department of Neurosurgery, Medical College of Georgia, Augusta, Ga., USA
email Corresponding Author

Krishnan M. Dhandapani, PhD

Department of Neurosurgery

Medical College of Georgia

Augusta, GA 30912 (USA)

Tel. +1 706 721 8846, Fax +1 706 721 7619, E-Mail kdhandapani@mcg.edu

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Traumatic brain injury (TBI) is a leading cause of death and disability in the United States. Current medical therapies exhibit limited efficacy in reducing neurological injury and the prognosis for patients remains poor. While most research is focused on the direct protection of neuronal cells, non-neuronal cells, such as astrocytes, may exert an active role in the pathogenesis of TBI. Astrocytes, the predominant cell type in the human brain, are traditionally associated with providing only structural support within the CNS. However, recent work suggests astrocytes may regulate brain homeostasis and limit brain injury. In contrast, reactive astrocytes may also contribute to increased neuroinflammation, the development of cerebral edema, and elevated intracranial pressure, suggesting possible roles in exacerbating secondary brain injury following neurotrauma. The multiple, opposing roles for astrocytes following neurotrauma may have important implications for the design of directed therapeutics to limit neurological injury. As such, a primary focus of this review is to summarize the emerging evidence suggesting reactive astrocytes influence the response of the brain to TBI.

© 2008 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: February 05, 2008
Issue release date: February 2008

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 0

ISSN: 1424-862X (Print)
eISSN: 1424-8638 (Online)

For additional information: http://www.karger.com/NSG

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